Key result
In vitro incubation of VLDL with hepatic lipase caused >80% hydrolysis of VLDL-triglycerides, and nascent VLDL disappeared faster than plasma VLDL during liver perfusion (half-life 56.2 vs 125.0 min).
Hepatic lipase has the capacity to hydrolyse VLDL-lipids and the liver can degrade VLDL particles, but these activities are depressed by plasma, suggesting previous plasma-free in vitro studies may need re-examination.
Plasma may inhibit hepatic lipase VLDL hydrolysis; hypothesis-generating for lipoprotein metabolism and requires validation in physiological models.
The role of the liver and of a heparin-releasable liver lipase in the metabolism of very low density lipoprotein (VLDL) was investigated in vitro and during recycling rat liver perfusion. Rat plasma VLDL and nascent hepatic VLDL were labelled biosynthetically in their lipid moieties. Incubation in vitro of VLDL with the lipase caused hydrolysis of VLDL-triglycerides (greater than 80%) and VLDL-phosphatidylcholine (greater than 30%). Nascent VLDL was a better substrate for the enzyme. The hydrolytic activities were inhibited by 70--90% when rat plasma (10--30 vol%) was added to the incubation mixture. VLDL-triglycerides and cholesterol esters were taken up by the liver during 180 min recycling perfusion. The rate of disappearance of nascent VLDL was faster than that of plasma VLDL (half-life times of 56.2 +/- 13.9 and 125.0 +/- 24.8 min respectively). Injection of heparin into the perfusion medium caused accelerated uptake of the hydrolysed VLDL-triglyceride by the liver. Addition of plasma (d greater than 1.006 g/ml) to the perfusion at a concentration of 10 vol% delayed the rate of disappearance of VLDL from the perfusate by about 50--75%. These studies have established the capacity of the hepatic lipase to hydrolyse VLDL-lipids and the ability of the liver to degrade nascent and plasma VLDL particles. These two activities, however, are depressed by plasma and therefore previous studies of VLDL metabolism may have to be re-examined when based on incubations or perfusions in the absence of plasma.
No takes yet. Share an insight, caveat, or question.
Berry et al. (1981) studied VLDL metabolism. Heparin-releasable liver lipase and liver perfusion was evaluated on Hydrolysis of VLDL-triglycerides and rate of disappearance of VLDL. In vitro incubation of VLDL with hepatic lipase caused >80% hydrolysis of VLDL-triglycerides, and nascent VLDL disappeared faster than plasma VLDL during liver perfusion (half-life 56.2 vs 125.0 min).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: